Abstract:The present study was designed to investigate the effect of MetVO-salen in ameliorating diabetes and oxidative stress in the pancreas of diabetic rats. Streptozotocin (STZ)-induced diabetic rats were treated with MetVO-salen complex intraperitonially (0.3 and 0.6 mg/kg) thrice a week and continued for 8 weeks. Total cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides in serum, and blood glucose were estimated. Furthermore, oxidative stress in rats was also investigated in terms of superoxide… Show more
“…Oxidative stress depicts the existence of products called free radicals and reactive oxygen species (ROS) formed under normal physiological conditions but become deleterious when not being quenched by the antioxidant systems (Fang et al 2002). When the balance is disrupted towards an over abundance of ROS, oxidative stress (OS) occurs in STZ induced diabetic rats (Roy et al 2011). Oxidative stress plays a role in the development of diabetic complications (Sexton and Jarow 1997).…”
Section: Discussionmentioning
confidence: 99%
“…It is one of the most commonly used substances to induce diabetes in experimental animals (Szkudelski 2001). Streptozotocin causes alkylation or breakage of DNA strands and a consequent increase in the activity of poly-ADP-ribose synthetase, an enzyme depleting the NAD + in β cells, leading to energy deprivation and finally apoptosis of the β cells of the pancreas (Roy et al 2011) and in the diabetic rat testis (Guneli et al 2008).…”
The aim of this study was to investigate the protective effect of naringenin on oxidative stress, on proinflammatorycytokines like TGF-β1, IL-1β and on programmed cell death in the testicular damage resultingfrom streptozotocin (STZ) induced diabetes in rats. Diabetes was induced by a single intraperitoneal injectionof STZ (50 mg/kg), and the rats were treated with naringenin (5 mg/kg and 10 mg/kg) administered oncea day orally for 10 weeks, starting 3 days after the STZ injection. At the end of the study, all animalswere sacrificed. Testis tissue and blood samples were collected for the assessment of sperm parameters, andfor biochemical and histopathological analysis. Naringenin treatment significantly decreased the levels ofelevated tissue TBARS (thio-barbituric acid) and increased the superoxide dismutase (SOD), catalase andglutathione peroxidase (GPx) enzyme activities in the testis tissues. The naringenin-treated rats in the diabeticgroup showed an improved histological appearance, sperm parameters, and serum testosterone levels, alongwith a decrement of terminal dUTP nick end-labeling (TUNEL) detected program cell death and a reducedover expression of TGF-β1, IL-1β in Sertoli cells and Leydig cells. These results suggest that naringeninis a food supplement potentially beneficial in reducing testicular damage in diabetic rats by decreasing theoxidative stress related to programmed cell death
“…Oxidative stress depicts the existence of products called free radicals and reactive oxygen species (ROS) formed under normal physiological conditions but become deleterious when not being quenched by the antioxidant systems (Fang et al 2002). When the balance is disrupted towards an over abundance of ROS, oxidative stress (OS) occurs in STZ induced diabetic rats (Roy et al 2011). Oxidative stress plays a role in the development of diabetic complications (Sexton and Jarow 1997).…”
Section: Discussionmentioning
confidence: 99%
“…It is one of the most commonly used substances to induce diabetes in experimental animals (Szkudelski 2001). Streptozotocin causes alkylation or breakage of DNA strands and a consequent increase in the activity of poly-ADP-ribose synthetase, an enzyme depleting the NAD + in β cells, leading to energy deprivation and finally apoptosis of the β cells of the pancreas (Roy et al 2011) and in the diabetic rat testis (Guneli et al 2008).…”
The aim of this study was to investigate the protective effect of naringenin on oxidative stress, on proinflammatorycytokines like TGF-β1, IL-1β and on programmed cell death in the testicular damage resultingfrom streptozotocin (STZ) induced diabetes in rats. Diabetes was induced by a single intraperitoneal injectionof STZ (50 mg/kg), and the rats were treated with naringenin (5 mg/kg and 10 mg/kg) administered oncea day orally for 10 weeks, starting 3 days after the STZ injection. At the end of the study, all animalswere sacrificed. Testis tissue and blood samples were collected for the assessment of sperm parameters, andfor biochemical and histopathological analysis. Naringenin treatment significantly decreased the levels ofelevated tissue TBARS (thio-barbituric acid) and increased the superoxide dismutase (SOD), catalase andglutathione peroxidase (GPx) enzyme activities in the testis tissues. The naringenin-treated rats in the diabeticgroup showed an improved histological appearance, sperm parameters, and serum testosterone levels, alongwith a decrement of terminal dUTP nick end-labeling (TUNEL) detected program cell death and a reducedover expression of TGF-β1, IL-1β in Sertoli cells and Leydig cells. These results suggest that naringeninis a food supplement potentially beneficial in reducing testicular damage in diabetic rats by decreasing theoxidative stress related to programmed cell death
“…conducted as reported previously (48). In brief, paraffin sections (3 µM) from the pancreatic tissues originally fixed in buffered formalin were deparaffinized and rehydrated, and heated in citrate buffer (pH 6.0) for 20 min.…”
Section: Immunohistochemical Analysis Of Enos Immunohistochemical Dementioning
Carbon monoxide (CO) is known as an essential gaseous messenger that regulates a wide array of physiological and pathological processes, similar to nitric oxide (NO) and hydrogen sulfide. The aim of the present study was to elucidate the potential role of CO in Ca(2+) homeostasis and to explore the underlying mechanisms in pancreatic acinar cells. The exogenous application of a CO-releasing molecule dose-dependently increased intracellular Ca(2+) concentration ([Ca(2+)]i). A heme oxygenase (HO) inducer increased [Ca(2+)]i in a concentration-dependent manner, and the increase was diminished by an HO inhibitor. The CO-induced [Ca(2+)]i increase persisted in the absence of extracellular Ca(2+), indicating that Ca(2+) release is the initial source for the increase. The inhibition of G protein, phospholipase C (PLC), and inositol 1,4,5-trisphosphate (IP3) receptor diminished the CO-induced [Ca(2+)]i increase. CO upregulated endothelial nitric oxide synthase (eNOS) expression and stimulated NO production, and NOS inhibitor, calmodulin inhibitor, or the absence of extracellular Ca(2+) eliminated the latter response. Blocking the phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) pathway abolished CO-induced NO production. Pretreatment with an NOS inhibitor, NO scavenger, or soluble guanylate cyclase inhibitor, did not affect the CO-induced [Ca(2+)]i increase, indicating that NO, soluble guanylate cyclase, and cyclic guanosine 5'-monophosphate are not involved in the CO-induced [Ca(2+)]i increase. CO inhibited the secretory responses to CCK-octapeptide or carbachol. We conclude that CO acts as a regulator not only for [Ca(2+)]i homeostasis via a PLC-IP3-IP3 receptor cascade but also for NO production via the calmodulin and PI3K-Akt/PKB pathway, and both CO and NO interact. Moreover, CO may provide potential therapy to ameliorate acute pancreatitis by inhibiting amylase secretion.
“…16 Salen type oxidovanadium complexes were found to exhibit insulin-mimetic and proteintyrosine phosphatase (PTP) inhibiting behavior. [17][18][19][20][21][22] Interestingly, oxidovanadium(IV) salen-type complexes were found to exist in either monomeric or polymeric forms in the solid state. 23,24 Oxidovanadium(IV) species with structures consisting of infinite polymeric chains bonded through V-O-V bridges are orange, brown or even black while the monomeric square pyramidal oxidovanadium(IV) species are usually green.…”
Oxidovanadium(IV) complexes with substituted chiral tetradentate dianionic N,N'-bis-o-hydroxybenzylidene-1,2-propylenediamines were synthesized and their physicochemical properties were characterized using single crystal X-ray diffraction, elemental analysis, ATR FTIR, UV-VIS and EPR spectroscopy, cyclic voltammetry, spectroelectrochemistry and preliminary in vitro protein-tyrosine phosphatase inhibition activity studies. Different 5-substituents in the salicylaldehyde (condensed with 1,2-diaminopropane; 2 : 1) were tested, namely 5-Br (complex 1), 5-Cl (2), 5-NO2 (3) and 5-OCH3 (4). The crystal structures of 1 and 2 show square pyramidal coordination of vanadium and parallel arrangement of monomeric exo isomers in supramolecular dimers. The halogen-halogen interaction of substituents in 5,5'-positions leads to weakening of axial interaction between phenolate O and V in 2, compared to 1. The Br atom takes part in halogen bonding with a vanadyl group in 1. Complex 3 has a linear polymeric structure with a V-O-V asymmetric bridge motif (IR absorption band at 873 cm(-1), separated d-d bands and broad EPR band structure in frozen solution pointing to oligomeric nature) while 4 is monomeric (V=O stretching at 976 cm(-1), broad d-d band structure). Redox potentials of the V(4+)/V(5+) couple lie in the range of -0.14 to 0.21 V (vs. Fc/Fc(+)) and show substantial dependence on the electron withdrawing properties of the substituents. The charge transfer character of the bands present in the range 365-395 nm was confirmed based on UV-VIS spectroelectrochemical experiments. Different assemblies of complex molecules are influenced by the electron withdrawing properties of the 5,5'-substituents, leading to supramolecular dimers (1, 2 and 4) and linear polymeric self-assembly (3). An in vitro study of representative complex 1 showed protein tyrosine phosphatase activity inhibition higher than that of suramin but lower than those of oxidovanadium(IV) sulphate and bis(maltolato)oxidovanadium(IV).
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